Subclinical and clinical presentation of Kounis syndrome: Another cause of troponin elevation?

Abstract

The development of acute coronary syndrome with ST-segmentelevation as a consequence of an allergic reaction has been describedfor patients with known coronary artery disease, as well for patientswith normal coronary arteries ( type II and type I variants of Kounissyndrome) [1–3], due to release of inflammatory factors and theirinfluence on epicardial heart vessels. However, the strict release ofhigh sensitivity cardiac troponins during an allergic reaction, withoutthe typical clinical and laboratory characteristics of an acute coronarysyndrome has not been described and may implicate a direct primaryallergic myocardial injury.The firstpatient concernsa 70-year-old male with a medical historyof an allergic reaction due to hymenoptera bite (hypotension andgeneralized rash) twenty years ago and a history of chronic obstructivepulmonary disease under treatment with ipratropium 40 mcg/qid andbudesonide400 mcg/bid.Thepatientwashypertensivetakingvalsartan160 mg/day, was dyslipidemic without any treatment but he wasreceiving aspirin 100 mg/day. Following a recent hymenoptera bite hedeveloped again intolerable generalized pruritus but without any othersymptom. Because of his suffering and his past medical history, he wasadmitted to our hospital. On admission, he had normal vital signs andoxygen saturation, reduced respiratory sounds without additional tones,while, in laboratory tests recorded mild leukocytosis with elevatedpolymorphonuclear percentage and normal high sensitivity cardiactroponin levels. The patient's electrocardiogram showed nonspeci ficST-Tchanges in I and aVL leads, compared to old electrocardiograms. Hereceived dimetinden maleate 0.1 mg/kg and hydrocortizone 250 mgwithagradualrecessionofsymptoms.Becauseofhismedicalhistoryhewas held and observed for the possible occurrence of delayedhypersensitivity. However, 12 h after the bite, an elevation of troponinI levels at 0.38 ng/mL (normal limits below 0,1 ng/mL) was detected,with concomitant increase in the enzyme CK-MB (26 iu/mL), withoutincreasing of other cardiac enzymes. Serial electrocardiograms showedno difference compared with that on admission. Cardiac ultrasoundrevealed no segmental cardiac wall hypokinesis, ventricular hypertro-phy, valvulopathies, systolic heart failure, or, apical ballooning. He wastreated with clopidogrel 75 mg/day, valsartan 160 mg/day, diltiazem60 mg/tid, atorvostatin 40 mg/day and desloratadine 5 mg/day. Aftermonitoring for 48 h he was discharged voluntarily, being asymptomaticwith recommendations for scintigraphic myocardial perfusion test.Thesecondpatientconcernsa60-year-oldwomanwhowasadmittedtoourhospitalforanelectiveorthopedicprocedure,speci fically,foratotalkneearthroplastyduetoseriousosteoarthritisofherleftknee.Thesameoperation was already performed for her right knee 2 years previously.She had a known history of dyslipidemia, hypothyroidism, depressivedisorder and venous insufficiency and was taking the relative medica-tion. There was a previous history of major allergic reaction tocefuroximeasshehaddevelopedwidespreadrash,itchingandshortnessof breath after the initiation of antibiotic for urinary tract infection. Shedid not mention anyother signi ficant past medical historyand no familyhistory of coronary disease. Her laboratory examinations revealed mildanemia due to known heterozygous b-thalassemia. Her blood glucoselevels were slightly above normal that it was not known and consideredto be due to stress-induced hyperglycemia. The rest blood examinationsand chest radiogram were normal. On preoperational assessment,cardiovascular system was normal and her electrocardiogram did notshow any specificabnormality(Fig. 1). On the third day after surgery,cefuroximewasadministered,accidentally,byintravenousinfusion.Soonafter the injection she became pale, cold and sweaty and her mentalstatus altered. She also complained of severe retrosternal pain that wasradiating to her left arm. Her blood pressure dropped down to 65/40 mm Hgandherheartratereached114 bpm.Anelectrocardiogramwasperformed immediately and revealed ST-segment elevation in leads II,III,AVFandreciprocalST-segmentdepressioninleadsI,AVL,V